Nicotinamide mononucleotide alleviates angiotensin II-induced human aortic smooth muscle cell senescence in a microphysiological model.

The occurrence and development of aortic aneurysms are accompanied by senescence of human aortic smooth muscle cells (HASMCs). As the mechanism of HASMC senescence has not been fully elucidated, the efficacy of various anti-senescence treatments varies. Decreased nicotinamide adenine dinucleotide (NAD+) levels are one of the mechanisms of cell senescence, and there is a lack of evidence on whether increasing NAD+ levels could alleviate HASMC senescence and further retard the progression of aortic aneurysms.